Dysautonomia is highly correlated with progressive CHF and renal disease such as those due to complications of diabetes. The correlation is due in significant part to side effects of various aggressive and long-term pharmacological treatments for CHF and diabetes. For example, diuretics are a mainstay of many CHF treatment regiments and orthostatic hypotension is known to be a progressive effect of excessive diuresis. More specifically, ACE inhibitors are known to cause or to worsen orthostatic hypotension.
With respect to the mechanics of underlying various orthostatic responses, consider that, in a supine position, approximately 25% to 30% of the circulating blood resides in the thorax. When a person assumes an upright position from a supine position, a gravity-mediated downward displacement of 300 ml to 800 ml of blood occurs to the abdomen and extremities. A change to an upright position thus causes a drop in blood volume of about 25% to 30% for regions that were flush with blood in the supine position, with 50% of this change occurring typically in the first few seconds of standing. This rapid redistribution of blood causes a decline of venous return to the heart and a decrease in cardiac filling pressure. In turn, stroke volume, and therefore cardiac output, declines approximately 40% due to the decline in venous return. In a normal individual, the decreased venous return to the heart can effect circulation in a manner that triggers baroreceptors in the carotid arteries and in the aortic arch, which, in turn, stimulate a sympathetic response and inhibit a parasympathetic response. Arteriolar constriction, venous constriction, increased skeletal muscle tone, and an increased heart rate are the normal hemodynamic responses to increased sympathetic tone caused by a drop in arterial pressure and cardiac output. Orthostatic stabilization is normally achieved in one minute or less, with a gradual tapering of heart rate.
With dysautonomia, the sympathetic nervous system may fail to respond adequately to decreasing blood pressure and, consequently, heart rate may not increase. This type of failure is an example characteristic of progressing dysautonomia. A patient with an inability to adjust to such position changes (i.e., impaired orthostatic stabilization) is often diagnosed as having orthostatic hypotension. If severe or otherwise problematic, a patient may be fitted with a pacing device capable of compensating for inadequate orthostatic control.
While various pacemakers are capable of compensating for inadequate orthostatic control, usually via enhanced rate responsive pacing (see, e.g., U.S. Pat. No. 6,351,642 and PACE 2000; 23 [Pt II]: 1809-1811, which are incorporated by reference herein), a need exists for improved mechanisms, especially for patients with progressing CHF. In particular, a need exists for algorithms that can respond to conditions prior to, during or after a change in position. As described herein, various exemplary methods, devices, systems, etc., address these need or other needs.